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1  initially focused on the more erythemogenic ultraviolet B.
2 t A, broadband ultraviolet B, and narrowband ultraviolet B.
3 e consisting of 98.8% ultraviolet A and 1.2% ultraviolet B.
4 ated tumor necrosis factor alpha response to ultraviolet B.
5 do not completely protect keratinocytes from ultraviolet B.
6  to undergo apoptosis after irradiation with ultraviolet B.
7 more readily inhibited at higher fluences of ultraviolet B.
8 50 1B1 in human skin, and their induction by ultraviolet-B.
9 ling from perches receiving higher levels of ultraviolet-B.
10                 This study demonstrates that ultraviolet B (280-320 nM) irradiation with physiologic
11 sun protection factor 15) offering primarily ultraviolet B (280-320 nm) protection.
12 yses revealed that exposure of human skin to ultraviolet-B (4 minimal erythema doses) resulted in enh
13                                              Ultraviolet B (40 mJ per cm2) significantly inhibited cu
14                     After low daily doses of ultraviolet B (6-4) photoproduct repair was most affecte
15        We found that relatively low doses of ultraviolet-B (62.5-500 mJ per cm2) caused dose-dependen
16 d showed that the sunscreen was primarily an ultraviolet B absorber, with relatively poor absorption
17 tive oxygen species generated in response to ultraviolet B also contribute to this phosphorylation.
18                                              Ultraviolet B also induces perinuclear cytoplasmic reloc
19 rradiated skin to an acute "sunburn dose" of ultraviolet-B also produced significant epidermal hyperp
20 moters, including a striking synergy between ultraviolet B and added interleukin-1alpha in the induct
21  technological advances including narrowband ultraviolet B and excimer laser.
22 s been used successfully in combination with ultraviolet B and psoralen plus ultraviolet A.
23 res of nor-mal keratinocytes were exposed to ultraviolet B and showed a dose-dependent increase in nu
24 lated to offer equivalent protection against ultraviolet B and ultraviolet A.
25  cm2 ultraviolet A, 100 mJ per cm2 broadband ultraviolet B, and 3.0 J per cm2 narrowband ultraviolet
26  plants were experimentally exposed to wind, ultraviolet B, and grown in large pots in growth chamber
27  ultraviolet B, and 3.0 J per cm2 narrowband ultraviolet B, and its stability was compared with sampl
28 ed upon exposure to ultraviolet A, broadband ultraviolet B, and narrowband ultraviolet B.
29 oxidant N-acetyl cysteine partially inhibits ultraviolet B-and oxidant-induced 27 kDa heat shock prot
30  was observed following exposure to doses of ultraviolet-B as low as 10 mJ per cm2.
31 n skin but are primarily designed to prevent ultraviolet-B-associated burning and damage.
32 atients exposed to high levels of tar and/or ultraviolet B before a first squamous cell carcinoma wer
33                      Interleukin-1alpha plus ultraviolet B caused a remarkable 300-fold increase in -
34                         When irradiated with ultraviolet-B, cells synchronized in G1 with mimosine di
35 resent at 44.3 ng per ml (SEM 6.2) following ultraviolet B compared with 26.0 ng per ml (SEM 8.0) in
36 synthesis of NO is induced by lower doses of ultraviolet B compared with that of prostaglandin E2.
37 ir positions longer on perches receiving low ultraviolet-B compared to perches receiving even slightl
38 ta from cancer genomes clearly implicate the ultraviolet B component of sunlight in melanoma skin can
39                               In response to ultraviolet B damage, keratinocytes undergo apoptosis to
40 nt-independent manner associated with direct ultraviolet B DNA damage.
41 when organotypic mixtures were exposed to an ultraviolet B dose of 50 mJ per cm2, intraepithelial tum
42 protected skin (buttock site) resulted in an ultraviolet-B dose-dependent (0-4 minimal erythema doses
43 ough degradation, was induced in vivo by low ultraviolet B doses but was suppressed at erythemal dose
44 oxo-dG in normal human skin keratinocytes at ultraviolet-B doses relevant to human skin exposure.
45 odes with narrow-band compared to broad-band ultraviolet B, even when treatments are based on predete
46 the basal cell layer of the epidermis in non-ultraviolet-B exposed skin, whereas cytochrome P450 1B1
47 e protected from wind, herbivore attack, and ultraviolet B exposure and grown in restricted rooting v
48              These findings demonstrate that ultraviolet B exposure can induce the intraepithelial ex
49 sages to exogenous interleukin-1 alpha after ultraviolet B exposure.
50 Northern Europe where residents have reduced ultraviolet-B exposure and tend to have light skin color
51 yclin D1 associated kinase activity, whereas ultraviolet-B exposure had no effect on cyclin-dependent
52  higher than customary are required if solar ultraviolet-B exposure is low.
53                                 We show that ultraviolet-B exposure of human epidermoid carcinoma A43
54 kin tumorigenesis, we assessed the effect of ultraviolet-B exposure on cell cycle progression of tran
55                                              Ultraviolet-B exposure to solar-ultraviolet-protected sk
56 rization was greatly increased after chronic ultraviolet-B exposure with a significant increase of bo
57 ty incidence was associated with female sex, Ultraviolet-B exposure, and a history of diabetes.
58    One formulation contained the established ultraviolet B filter octyl methoxycinnamate, whereas the
59  sunscreen containing both ultraviolet A and ultraviolet B filters totally blocked ultraviolet-induce
60  the highest quintile of cumulative midrange ultraviolet B flux exposure versus the lowest quintile w
61      Attributable risks did not vary by age, ultraviolet B flux or hours outdoors.
62 t A and other ultraviolet exposures, such as ultraviolet B for skin cancer development in psoralen +
63                Psoriasis may be treated with ultraviolet B from lamps that have a broad emission spec
64 hemal response to narrow-band and broad-band ultraviolet B in 12 patients with psoriasis.
65 rative response of II-4 cells was altered by ultraviolet B in organotypic cultures.
66  environmental insult, our data suggest that ultraviolet B, in addition to initiating recognized cyto
67 f other carcinogenic exposures, particularly ultraviolet B, in the development of skin cancer.
68 ydrogen peroxide is an important mediator of ultraviolet B induced phosphorylation of the epidermal g
69 cultured JB6 cells, C3G was able to scavenge ultraviolet B-induced *OH and O2-* radicals.
70 e is thus the major transduction pathway for ultraviolet B-induced 27 kDa heat shock protein phosphor
71 ure, and this coincides with the reversal of ultraviolet B-induced actin reorganization.
72 89 blocks MSK1 activity but does not inhibit ultraviolet B-induced activation of MAP kinases p70/85(S
73 oyltransferase, significantly attenuated the ultraviolet B-induced apoptosis in a caspase-3-independe
74 sponsible pathway for ceramide generation in ultraviolet B-induced apoptosis of cultured normal human
75 increased de novo ceramide synthesis signals ultraviolet B-induced apoptosis, by a pathway independen
76 -chloromethyl-ketone) further attenuated the ultraviolet B-induced apoptosis.
77 ix times more sensitive than normal cells to ultraviolet B-induced apoptosis.
78 approximately 2-fold shallower than that for ultraviolet B-induced erythema.
79  cancer is also thought to be due in part to ultraviolet B-induced impairment of immune responses.
80 cid, and phosphorylcholine revealed that the ultraviolet B-induced increase in ceramide results prima
81 y carotenoids were efficient in reducing the ultraviolet B-induced increases in the percentage of pro
82                                          The ultraviolet B-induced phosphorylation is not affected by
83                                          The ultraviolet B-induced phosphorylation is reversible, ret
84 ow that both ERKs and p38 kinase may mediate ultraviolet B-induced phosphorylation of H3 at serine 10
85  p38 kinase inhibitor, efficiently inhibited ultraviolet B-induced phosphorylation of H3.
86 l or C-terminal mutant MSK1 strongly blocked ultraviolet B-induced phosphorylation of histone H3 at s
87     These data illustrate that MSK1 mediates ultraviolet B-induced phosphorylation of histone H3 at s
88 f the nucleosomal response, totally inhibits ultraviolet B-induced phosphorylation of histone H3 at s
89  protein kinases MAP kinases are involved in ultraviolet B-induced phosphorylation of histone H3 at s
90                                              Ultraviolet B-induced skin cancer is also thought to be
91  which was confirmed histologically, whereas ultraviolet B-induced tanning of light-skinned swine was
92  suggested that II-4 cells were resistant to ultraviolet-B-induced alterations, which allowed these i
93 ed survivin expression and protected against ultraviolet-B-induced apoptosis.
94     Taken together, our results suggest that ultraviolet-B-induced cell cycle arrest in A431 cells is
95 ther inhibition of angiogenesis may diminish ultraviolet-B-induced cutaneous damage, wild-type and tr
96 , it is not known whether PAF is involved in ultraviolet-B-induced epidermal cell cytokine production
97 udies examined the role of the PAF system in ultraviolet-B-induced epidermal cell interleukin-8 biosy
98                                              Ultraviolet-B-induced erythema (one, two, or four times
99                    Objective measurements of ultraviolet-B-induced erythema were performed using refl
100 xide also made a significant contribution to ultraviolet-B-induced erythema.
101 ling, which triggers increased pigmentation, ultraviolet-B-induced G1-like cell cycle arrest and cont
102                                           An ultraviolet-B-induced increase in H2O2 was observed in n
103                          DNA is a target for ultraviolet-B-induced inhibition of contact hypersensiti
104 sts inhibited both carbamoyl-PAF-induced and ultraviolet-B-induced interleukin-8 production in the PA
105  Ascorbic acid-6-palmitate strongly promoted ultraviolet-B-induced lipid peroxidation, c-Jun N-termin
106 ould make the human skin more susceptible to ultraviolet-B-induced skin cancers or allergic and irrit
107 f the cutaneous vascular system in mediating ultraviolet-B-induced skin damage and suggest inhibition
108 e of the vascular system in the mediation of ultraviolet-B-induced skin damage, we performed quantita
109 rder to identify potential novel targets for ultraviolet-B-induced skin tumorigenesis, we assessed th
110 Because tumor necrosis factor alpha mediates ultraviolet-B-induced suppression of contact hypersensit
111 the exogenous interleukin-12 totally blocked ultraviolet-B-induced tumor necrosis factor alpha produc
112 that anti-interleukin-12 antibodies enhanced ultraviolet-B-induced tumor necrosis factor alpha secret
113                                              Ultraviolet-B induction of both cytochrome P450 1A1 and
114 ysis of their negative regulators, being the ULTRAVIOLET-B-INSENSITIVE4 protein and the DP-E2F-Like1
115 ight exposure and resembled that observed in ultraviolet-B-irradiated mice.
116 during oxidative stress, its accumulation in ultraviolet-B-irradiated normal human epidermal keratino
117                                              Ultraviolet-B-irradiated thrombospondin-1 transgenic mic
118         Skin cancer arising from exposure to ultraviolet B irradiation (UVB) from the sun is a promin
119                                              Ultraviolet B irradiation and traditional Chinese medici
120 ein and zeaxanthin diminishes the effects of ultraviolet B irradiation by reducing acute inflammatory
121 ison ivy or poison oak, and chronic low-dose ultraviolet B irradiation can damage the skin.
122    These data indicate that 90 mJ per cm2 of ultraviolet B irradiation induces a DNA damage response,
123                                              Ultraviolet B irradiation is thought to enable skin canc
124                                              Ultraviolet B irradiation of PAF-receptor-expressing KB
125 complish this, we have studied the effect of ultraviolet B irradiation on organotypic cultures that w
126 f this study was to characterize the role of ultraviolet B irradiation on the intraepithelial expansi
127 ct inhibited AP-1 transactivation induced by ultraviolet B irradiation or TPA in JB6 cells and AP-1-l
128                                      Chronic ultraviolet B irradiation significantly reduced the init
129  synthase (i.e., 1.7-fold increase 8 h after ultraviolet B irradiation), whereas serine palmitoyltran
130 ame evident in a time-dependent manner after ultraviolet B irradiation, in parallel with activation o
131     Furthermore, guinea pigs were exposed to ultraviolet B irradiation, known to enhance transport of
132 th cdk-2 and cdk-4 at 3-24 h and 6-24 h post-ultraviolet B irradiation, respectively.
133  and zeaxanthin in the cutaneous response to ultraviolet B irradiation.
134  levels of reactive oxygen species following ultraviolet B irradiation.
135                                      Chronic ultraviolet-B irradiation of the skin results in epiderm
136 of topical application of pTpT with those of ultraviolet-B irradiation on C57BL/6 mice sensitized to
137  thrombospondin-1 were subjected to the same ultraviolet-B irradiation regimen.
138                 Mice pretreated with pTpT or ultraviolet-B irradiation showed markedly suppressed ear
139 actor alpha promoter, we examined effects of ultraviolet-B irradiation versus intradermal injection o
140 ate membranes, our data indicate that, after ultraviolet-B irradiation, H2O2 migrates from the cytoso
141 rrest in transformed keratinocytes following ultraviolet-B irradiation.
142 taneous blood vessels of mice after 10 wk of ultraviolet-B irradiation.
143 in 2 studies, subjects had received solar or ultraviolet-B irradiation.
144                              Transmission of ultraviolet B is reduced by 67%-87% through vehicle and
145 er frogs on perches receiving relatively low ultraviolet-B levels maintained their positions for long
146 ed to perches receiving even slightly higher ultraviolet-B levels.
147 neous changes occur from chronic exposure to ultraviolet B light (290 to 320 nm) associated with sunb
148                                              Ultraviolet B light (UV-B; 280-320 nm) perception and si
149                                              Ultraviolet B light (UVB) causes cutaneous inflammation
150                                              Ultraviolet B light (UVB) is a common cause of human ski
151  histone H3 was enhanced by stimulation with ultraviolet B light (UVB) or epidermal growth factor (EG
152 el exercise decreased body fat and inhibited ultraviolet B light (UVB)-induced carcinogenesis in the
153        Treatment of SKH-1 hairless mice with ultraviolet B light (UVB; 30 mJ/cm(2)) twice a week for
154 entration >80 nmol/L in persons with limited ultraviolet B light exposure.
155                                              Ultraviolet B light induces EXO70H4 transcription in a C
156 idual cumulative lifetime ocular exposure to ultraviolet B light on cortical cataract risk for each l
157                                Surprisingly, ultraviolet B light or Benzo(a)pyrene exposure of skin s
158  for vitamin D3 precursors after exposure to ultraviolet B light we found that the conversion of 7-de
159 he form of methyl jasmonate, salicylic acid, ultraviolet B light, and wounding, chosen on the basis o
160             Persons with limited exposure to ultraviolet B light, including space travelers, may not
161 s acquired through diet and skin exposure to ultraviolet B light.
162 oduce vitamin D after repeated high doses of ultraviolet B light.
163                            Here we show that ultraviolet-B light (UV-B) perceived by the photorecepto
164 1 pal2 double mutants were more sensitive to ultraviolet-B light but more tolerant to drought than wi
165  3) There is new awareness of the hazards of ultraviolet-B light exposure in childhood and the subseq
166 ivin by RNA interference sensitizes cells to ultraviolet B-mediated apoptosis and results in enhanced
167 tes with ascorbic acid-6-palmitate inhibited ultraviolet-B-mediated activation of epidermal growth fa
168 adiation in skin and thus may act to augment ultraviolet-B-mediated production of cytokines such as i
169 her pTpT mimics the suppressive influence of ultraviolet-B on contact hypersensitivity, we compared t
170  that applying a sunscreen that contained an ultraviolet B only filter had no protective effect, wher
171                                        Solar ultraviolet B photons are absorbed by 7-dehydrocholester
172 atment of psoriasis in children, narrow band ultraviolet B phototherapy for atopic dermatitis and pso
173 on, daily treatment with a higher fluence of ultraviolet-B produced extensive hyperplasia and conside
174 sun protection factors (mainly indicative of ultraviolet B protection) quoted by the manufacturers (2
175                                 In contrast, ultraviolet B radiation (280-320 nm) initiates melanoma
176    Subjects who use a tanning bed that emits ultraviolet B radiation (290-315 nm) are likely to have
177  responses triggered by low fluence rates of ultraviolet B radiation (UV-B; 280-315 nm) are mediated
178                                              Ultraviolet B radiation (UVB) is a pro-oxidative stresso
179    To examine the association of myopia with ultraviolet B radiation (UVB; directly associated with t
180 response relation between ocular exposure to ultraviolet B radiation and cortical cataract were deriv
181 es for US cataract incidence of increases in ultraviolet B radiation due to ozone depletion.
182               Both the estimated exposure to ultraviolet B radiation during late pregnancy and the ma
183 (OH)D >/=50 nmol/L during periods of minimal ultraviolet B radiation exposure.
184 kin type and a greater likelihood of reduced ultraviolet B radiation exposure.
185 ated 3x per week for 12 wk with 15 kJ per m2 ultraviolet B radiation followed by application of the p
186                                              Ultraviolet B radiation has been shown to generate cutan
187 F receptor may be a pharmacologic target for ultraviolet B radiation in skin and thus may act to augm
188                                  Exposure to ultraviolet B radiation is an important trigger of both
189 mmatory cytokines synthesized in response to ultraviolet B radiation is the potent chemoattractant in
190 r in Antarctica at the McMurdo Station, when ultraviolet B radiation levels are essentially zero.
191  was subsequently exposed to acute, low-dose ultraviolet B radiation partially prevented tolerance in
192 own that chronic exposure to low fluences of ultraviolet B radiation reduced DNA repair capacity in m
193 dermal cell line A-431 with carbamoyl-PAF or ultraviolet B radiation resulted in interleukin-8 produc
194    When both cell lines were irradiated with ultraviolet B radiation, caspase 3 activity increased to
195 pic and exposure factors, including midrange ultraviolet B radiation, in our study populations.
196 uations, we subjected chemically- as well as ultraviolet B radiation-induced squamous papillomas in S
197 iet for 2 wk were exposed to single doses of ultraviolet B radiation.
198 pevine during development and in response to ultraviolet B radiation.
199 altered during epidermal proliferation after ultraviolet B radiation.
200 le in the local immune aberrations caused by ultraviolet B radiation.
201 to the tolerance promoted by acute, low-dose ultraviolet B radiation.
202  to the tolerance induced by acute, low-dose ultraviolet B radiation.
203 rsensitivity induction after acute, low-dose ultraviolet B radiation.
204 r and characteristic of DNA damage caused by ultraviolet B radiation.
205 uman epidermal keratinocytes were exposed to ultraviolet-B radiation (290-320 nm).
206 ither oral administration of vitamin D(3) or ultraviolet-B radiation across a broad range of inputs.
207                                      Surface ultraviolet-B radiation and atmospheric CO2 concentratio
208                                      Ambient ultraviolet-B radiation can harm amphibian eggs, larvae
209  immortalized mouse keratinocytes exposed to ultraviolet-B radiation, we now report the induction of
210 se skin after chronic and acute exposures to ultraviolet-B radiation.
211 , delay the onset of skin tumors, and reduce ultraviolet-B-radiation-induced skin wrinkling.
212 that frogs called from perches receiving low ultraviolet-B regardless of perch height, and that frogs
213 ere down-regulated in cml42, and impaired in ultraviolet B resistance.
214 oredoxins, major latex protein-like protein, ULTRAVIOLET-B RESISTANCE8 photoreceptor) that contribute
215 ells of ultraviolet B-susceptible (C3H/HeN), ultraviolet B-resistant (C3H/HeJ), and mast-cell deficie
216  effector molecules, we asked if pTpT mimics ultraviolet-B's upregulatory influence on tumor necrosis
217 cular analyses demonstrate that WXR3 is ROOT ULTRAVIOLET B-SENSITIVE1 (RUS1), a member of the conserv
218 ild-type mice, indicating that 86-90% of the ultraviolet B signal for keratinocyte apoptosis involved
219 iption factors following irradiation with an ultraviolet B source and solar-simulated ultraviolet irr
220 ese agents also inhibited the forskolin- and ultraviolet B-stimulated promoter activities of these ge
221  loaded Fcepsilon receptors of mast cells of ultraviolet B-susceptible (C3H/HeN), ultraviolet B-resis
222 whether frogs at higher perches receive more ultraviolet-B than those calling from lower perches.
223 of these cells types to apoptosis induced by ultraviolet B, the tyrosine analog 4-tert-butylphenol, a
224                            Ultraviolet A and ultraviolet B transmission were measured through thin an
225 erleukin-8 mRNA and protein in comparison to ultraviolet-B-treated control KB cells.
226  this study, keratinocytes were treated with ultraviolet-B, ultraviolet-A, or sham irradiation, witho
227  epidermal and dermal measures compared with ultraviolet B under the conditions used.
228 s, and giving large doses of platelets while ultraviolet B (UV-B) or gamma irradiation decreased plat
229 f absorption by BrC in the UV and diminished ultraviolet B (UV-B) radiation reaching the surface.
230 nvolved in development and translation under ultraviolet B (UV-B) stress.
231                                              Ultraviolet-B (UV-B) light exposure further promotes the
232 ISTANCE LOCUS8 (UVR8) is a photoreceptor for ultraviolet-B (UV-B) light that initiates photomorphogen
233 ry changes in gene expression in response to ultraviolet-B (UV-B) light through an unknown mechanism.
234                                              Ultraviolet-B (UV-B) photons can cause substantial cellu
235                                          The ultraviolet-B (UV-B) photoreceptor UV RESISTANCE LOCUS 8
236                                              Ultraviolet-B (UV-B) radiation affects leaf growth in a
237 ough climatic changes, increased exposure to ultraviolet-B (UV-B) radiation and increased prevalence
238                                              Ultraviolet-B (UV-B) radiation can have a negative impac
239 nses are induced in the cells by exposure to ultraviolet-B (UV-B) radiation.
240 h the environment, including the response to ultraviolet-B (UV-B) stress.
241 anding the molecular mechanisms by which the ultraviolet-B (UV-B)-exposed cells are being protected a
242                                        Solar ultraviolet B (UVB) acts as both an initiator and promot
243  the keratinocyte machinery that responds to ultraviolet B (UVB) and functions critically to convert
244  comprising ~95% ultraviolet A (UVA) and ~5% ultraviolet B (UVB) at the Earth's surface, promotes mel
245              Epidemiological studies suggest ultraviolet B (UVB) component (290-320 nm) of sun light
246                                              Ultraviolet B (UVB) damage is recognized as the most imp
247                      The effects of a single ultraviolet B (UVB) exposure on hyaluronan content and m
248 longed nearly complete desiccation, and high ultraviolet B (UVB) exposure.
249 rradiation of human or murine epidermis with ultraviolet B (UVB) induces clones of p53-mutant keratin
250                                              Ultraviolet B (UVB) induces phosphorylation of histone H
251 on of two models of inflammatory pain, using ultraviolet B (UVB) irradiation alone and UVB irradiatio
252                                      Whereas ultraviolet B (UVB) irradiation of neonates yielded high
253 ctor for BCC is sun exposure, the ability of ultraviolet B (UVB) irradiation to activate PKD in prima
254                     In response to sublethal ultraviolet B (UVB) irradiation, human keratinocytes tra
255 en studied using pure ultraviolet A (UVA) or ultraviolet B (UVB) irradiation, the signaling pathways
256 two models of inflammatory pain that involve ultraviolet B (UVB) irradiation, which can employ periph
257 nogens and environmental stresses, including ultraviolet B (UVB) irradiation.
258 ed MIF(-/-) BALB/c mice to acute and chronic ultraviolet B (UVB) irradiation.
259       Apoptotic NIT-1 cells were prepared by ultraviolet B (UVB) irradiation.
260 A repair in normal human keratinocytes after ultraviolet B (UVB) irradiation.
261                                  Narrow-band ultraviolet B (UVB) is an effective treatment for psoria
262                                              Ultraviolet B (UVB) light is the principal aetiological
263 -quadruplex forming human telomeric DNA with ultraviolet B (UVB) light results in the formation of an
264                   In this study, by applying ultraviolet B (UVB) light, a physiologically relevant st
265                         When irradiated with ultraviolet B (UVB) light, K14/Bcl-2 mice developed abou
266                   We assessed the effects of ultraviolet B (UVB) on the p38 MAPK pathway and determin
267 factor activator protein 1 (AP-1) induced by ultraviolet B (UVB) or 12-O-tetradecanoylphorbol-13-acet
268                                          The ultraviolet B (UVB) portion (280-320 nm) of the ultravio
269                            Sunlight contains ultraviolet B (UVB) radiation (290-315 nm) that affects
270 min D3 is generated secondary to exposure to ultraviolet B (UVB) radiation (whether from the sun or f
271 igments provide efficient protection against ultraviolet B (UVB) radiation but DNA repair also plays
272                                              Ultraviolet B (UVB) radiation causes cutaneous inflammat
273                                  Exposure to ultraviolet B (UVB) radiation from the sun can result in
274 cer in the United States, where DNA-damaging ultraviolet B (UVB) radiation from the sun remains the m
275                      She was then exposed to ultraviolet B (UVB) radiation in a tanning bed wearing a
276                                        Solar ultraviolet B (UVB) radiation induces cutaneous ornithin
277  SIRT1 in skin cancer development induced by ultraviolet B (UVB) radiation is dependent on its gene d
278 ry processes induced in the skin by moderate ultraviolet B (UVB) radiation on central nervous system
279  fibroblasts with the pro-oxidative stressor ultraviolet B (UVB) radiation resulted in increased reac
280 elling response to midrange UVR (280-320 nm, ultraviolet B (UVB) radiation) and UVB suppression of co
281 In addition, we found that the proportion of ultraviolet B (UVB) radiation-induced C>T transitions di
282 D8+ T cells, using monoclonal antibodies, on ultraviolet B (UVB) radiation-induced inflammation and t
283 ared to wild-type mice following exposure to ultraviolet B (UVB) radiation.
284 and promoter-specific transactivation in the ultraviolet B (UVB) response.
285                                              Ultraviolet B (UVB) therapy, used for the treatment of p
286     SKH-1 hairless mice were irradiated with ultraviolet B (UVB) twice weekly for 20 weeks.
287 ) analysis of nuclear extracts prepared from ultraviolet B (UVB)- and N-methyl-N'-nitro-N-nitrosoguan
288                                              Ultraviolet B (UVB)-induced cyclooxygenase-2 (COX-2) exp
289 lyunsaturated fatty acids (n-3 PUFA) inhibit ultraviolet B (UVB)-induced inflammation and other infla
290 xpression is a likely contributing factor in ultraviolet B (UVB)-induced non-melanoma skin cancer (NM
291 ega-3 polyunsaturated fatty acids (PUFAs) on ultraviolet B (UVB)-induced skin inflammation and photoc
292 urally occurring flavonoid silibinin against ultraviolet B (UVB)-induced skin tumorigenesis.
293                         Transfusions (Tx) of Ultraviolet B (UVB)-irradiated peripheral blood mononucl
294 ern European subjects with multiple doses of ultraviolet B (UVB).
295 on assessed under basal conditions, or after ultraviolet-B (UVB) irradiation, or phorbol ester stimul
296 propriate response of human keratinocytes to ultraviolet-B (UVB) is dependent on the activation statu
297 lectin-3 mRNA was transiently upregulated in ultraviolet-B (UVB)-irradiated wild-type keratinocytes.
298 ta are, however, conflicting on the roles of ultraviolet B [UVB; 280-320 nanometers (nm)] and ultravi
299                       Both ultraviolet-A and ultraviolet-B were capable of inducing interleukin-12 pr
300 f the solar spectrum (320-400 nm), devoid of ultraviolet B, were equally effective in activating immu
301     Melanocytes were relatively resistant to ultraviolet B, whereas keratinocytes were unresponsive t

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